A 19-year-old woman presented with acute progressive generalized limb weakness and inability to ambulate, after a recent upper respiratory tract infection. Given the flaccid quadriparesis and preceding infection, Guillain-Barré syndrome (GBS) was initially considered. This case aims to illustrate the diagnostic challenges and the critical role of backward reasoning in differentiating GBS mimickers. Neurologic examination, electrodiagnostic studies, brain MRI, and hematologic testing were performed. Motor nerve conduction and late responses were normal, whereas sensory studies indicated pure distal sensory polyneuropathy. MRI revealed cervical spinal cord hyperintensities, and blood tests showed macrocytic anemia and low serum vitamin B12. The diagnosis of severe vitamin B12 deficiency was established. The patient received cobalamin replacement therapy, and significant clinical improvement was observed for a 3-month follow-up period. Vitamin B12 deficiency can mimic GBS, particularly in acute settings. Accurate clinical reasoning, including the application of backward reasoning when atypical findings emerge, is essential to avoid misdiagnosis and ensure timely treatment in patients with acute neurologic presentations.

Vincristine sulfate (VIN) is commonly employed as a cytotoxic agent in the treatment of hematological malignancies, particularly acute lymphoblastic leukaemia (ALL). However, its maximum therapeutic benefits have been hindered due to the dose-dependent neurotoxic effects it can induce, which traditionally manifest as autonomic and peripheral sensory-motor neuropathy. The innovative approach aimed to address VIN's neurotoxic limitations while preserving its therapeutic efficacy in combating hematological malignancies, including ALL. The liposomes were prepared using the reverse-phase evaporation method. This method involved the encapsulation of VIN within liposomes through a controlled evaporation process. Secondly, PEGylated liposomes were synthesized through PEGylation. The liposomes were examined using scanning electron spectroscopy, revealing a smooth and spherical surface morphology. The particle size of the liposomes ranged from 90±0.5 to 120±0.4 nm. The encapsulation efficiency of the liposomes was found to be 77.24% and the highest drug release reached 95% over 50 hours. Cytotoxicity studies demonstrated that the liposomal formulation exhibited a non-toxic nature. Furthermore, in an in-vivo cellular uptake study, the PEGylated liposomes showed efficient accumulation within tumor cells. The liposomal formulation demonstrated superior effectiveness in treating ALL compared to the pure form of the drug.

The objective of this review was to analyze the pathophysiological role of endoneurial inflammatory edema in initial stages of classic Guillain-Barré syndrome (GBS), arbitrarily divided into very early GBS (≤ 4 days after symptom onset) and early GBS (≤ 10 days). Classic GBS, with variable degree of flaccid and areflexic tetraparesis, encompasses demyelinating and axonal forms. Initial autopsy studies in early GBS have demonstrated that endoneurial inflammatory edema of proximal nerve trunks, particularly spinal nerves, is the outstanding lesion. Variable permeability of the blood-nerve barrier dictates such lesion topography. In proximal nerve trunks possessing epi-perineurium, edema may increase the endoneurial fluid pressure causing ischemic changes. Critical analysis the first pathological description of the axonal form GBS shows a combination of axonal degeneration and demyelination in spinal roots, and pure Wallerian-like degeneration in peripheral nerve trunks. This case might be reclassified as demyelinating GBS with secondary axonal degeneration. Both in acute motor axonal neuropathy and acute motor-sensory axonal neuropathy, Wallerian-like degeneration of motor fibers predominates in the distal part of ventral spinal roots abutting the dura mater, another feature re-emphasizing the pathogenic relevance of this area. Electrophysiological and imaging studies also point to a predominant alteration at the spinal nerve level, which is a hotspot in any early GBS subtype. Serum biomarkers of axonal damage, including neurofilament light chain and peripherin, are increased in the great majority of patients with any early GBS subtype; endoneurial ischemia of proximal nerve trunks could contribute to such axonal damage. It is concluded that inflammatory edema of proximal nerve trunks is an essential pathogenic event in early GBS, which has a tangible impact for accurate approach to the disease.

To describe the clinical, micronutrient, and electrophysiologic spectra and prognosis in patients with acute nutritional axonal neuropathy (ANAN). Patients with ANAN were identified between 1999 and 2020 by a retrospective review of our EMG database and electronic health records and categorized on clinical and electrodiagnostic grounds, as pure sensory, sensorimotor, or pure motor; and by risk factor (alcohol use disorder, bariatric surgery, or anorexia). Laboratory abnormalities were recorded including thiamine, vitamin B6, B12, and E, folate, and copper. Ambulatory and neuropathic pain status at last follow-up were recorded. Of 40 patients with ANAN, 21 had alcohol use disorder, 10 were anorexic, and 9 had recently undergone bariatric surgery. Their neuropathy was pure sensory in 14 (7 with low thiamine), sensorimotor in 23 (8 with low thiamine), and pure motor in 3 (1 with low thiamine). Vitamin B1 was most commonly low (85%), followed by vitamin B6 (77%) and folate (50%). The risk factor and neuropathy type were not associated with a particular micronutrient deficiency. Of the 37 patients who were seen in follow-up, only 13 (35%) were walking independently, and only 8 (22%) were pain free at the last follow-up visit at a mean of 22 months (range 2-88 months) from onset. The spectrum of ANAN is wide, ranging from: (1) a pure sensory neuropathy with areflexia, limb and gait ataxia, neuropathic pain, and unevocable sensory responses to (2) a motor axonal neuropathy with low-amplitude motor responses without conduction slowing, block, or dispersion, and (3) a mixed sensorimotor axonal polyneuropathy. Specific micronutrient deficiencies or risk factors do not predict neuropathy subtype. The subgroup of patients with ANAN with documented thiamine deficiency also range from pure sensory to pure motor, and only a minority have Wernicke encephalopathy. We do not know whether coexistent micronutrient deficiencies may help explain the wide clinical spectrum of thiamine-deficient ANAN. The prognosis of ANAN is guarded due to residual neuropathic pain and slow recovery of independent ambulation. Therefore, early recognition of patients at risk is important.

Parsonage-Turner syndrome (PTS) is an inflammatory disorder of the brachial plexus. Hypothesized underlying causes focus on immune-mediated processes, as more than half of patients present some antecedent event or possible predisposing condition, such as infection, vaccination, exercise, or surgery. Recently, PTS was reported following the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We aimed to investigate data on PTS triggered by SARS-CoV-2 infection to provide an extensive perspective on this pathology and to reveal what other, more specific, research questions can be further addressed. In addition, we aimed to highlight research gaps requiring further attention. We systematically reviewed two databases (LitCOVID and the World Health Organization database on COVID-19) to January 2023. We found 26 cases of PTS in patients with previous SARS-CoV-2 infection. The clinical and paraclinical spectrum was heterogeneous, ranging from classical PTS to pure sensory neuropathy, extended neuropathy, spinal accessory nerve involvement, and diaphragmatic palsy. Also, two familial cases were reported. Among them, 93.8% of patients had severe pain, 80.8% were reported to present a motor deficit, and 53.8% of patients presented muscle wasting. Paresthesia was noted in 46.2% of PTS individuals and a sensory loss was reported in 34.6% of patients. The present systematic review highlights the necessity of having a high index of suspicion of PTS in patients with previous SARS-CoV-2 infection, as the clinical manifestations can be variable. Also, there is a need for a standardized approach to investigation and reporting on PTS. Future studies should aim for a comprehensive assessment of patients. Factors including the baseline characteristics of the patients, evolution, and treatments should be consistently assessed across studies. In addition, a thorough differential diagnosis should be employed.